Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mice, Gcn2 Knockout mice, and Hri Knockout mice

ABSTRACT: Gene expression profile at Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mice, Gcn2 Knockout mice, and Hri Knockout mice

PROVIDER: PRJNA828131 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18819100_1.fastq.gz	Fastqsanger.gz
	SRR18819100_2.fastq.gz	Fastqsanger.gz
	SRR18819101_1.fastq.gz	Fastqsanger.gz
	SRR18819101_2.fastq.gz	Fastqsanger.gz
	SRR18819102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 42

Similar Datasets

Gene expression profile at Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mice, Gcn2 Knockout mice, and Hri Knockout mice

Project description:To study the mitochondrial stress response HRI-eIF2a-ATF4 signaling pathway in mitochondrial cardiomyopathy , we generated Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mcie, Gcn2 Knockout mcie, and Hri Knockout mcie

2022-04-21 | GSE201042 | GEO

Cytoplasmic proteotoxicity regulates HRI-dependent phosphorylation of eIF2a via the Hsp70-Bag3 module.

Project description:The major heat shock protein Hsp70 has been shown to form a complex with a scaffold protein Bag3, linking it to multiple signaling pathways. Via these interactions, the Hsp70-Bag3 module functions as a proteotoxicity sensor that controls cell signaling. Here, as a tool to identify signaling pathways regulated by this complex, we utilized JG-98, an allosteric inhibitor of Hsp70 that blocks its interaction with Bag3. Gene expression profiling followed by the pathway analysis indicated that a set of signaling pathways including the unfolded protein response (UPR) was activated by JG-98. Surprisingly, only the translation initiation factor eIF2a-associated branch of the UPR was activated under these conditions, while other UPR branches mediating induction of ER chaperones were not induced, suggesting that the response was not related to ER proteotoxicity and thus to ER-associated kinase PERK1. Indeed, induction of the UPR genes under these conditions was dependent on activation of a distinct cytoplasmic eIF2a kinase, HRI. We demonstrated that the Hsp70-Bag3 complex directly interacted with HRI and regulated phosphorylation of eIF2a upon induction of cytoplasmic proteotoxicity. Therefore, we uncovered a novel signaling response, which regulates cell death upon the buildup of abnormal protein species in cytoplasm via an Hsp70-Bag3-HRI-eIF2a axis.

2021-04-14 | GSE171440 | GEO

PTPMT1 is critical for both expansion and differentiation of activated CD8 T cells

Project description:To understand the function of PTPMT1 in CD8 T cells responses, we characterized the transcriptomes of activated CD8+ T cells from PTPMT1 wildtype and knockout mice

2023-11-21 | GSE216523 | GEO

Cytoplasmic proteotoxicity regulates HRI-dependent phosphorylation of eIF2a via the Hsp70-Bag3 module.

Project description:Cytoplasmic proteotoxicity regulates HRI-dependent phosphorylation of eIF2a via the Hsp70-Bag3 module.

| PRJNA719638 | ENA

Iron and Heme Coordinate Erythropoiesis through HRI-Mediated Regulation of Protein Translation and Gene Expression

Project description:Iron and heme play central roles in red blood cell production. However, the mechanisms by which iron and heme levels coordinate erythropoiesis remain incompletely understood. HRI is a heme-regulated kinase that controls translation by phosphorylating eIF2a. Here, we investigate the global impact of iron, heme and HRI on protein translation in vivo in murine primary erythroblasts using ribosome profiling. By defining the underlying changes in translation during iron and HRI deficiencies, we validate known regulators of this process, including Atf4, and identify novel pathways such as co-regulation of ribosomal protein mRNA translation. Surprisingly, we found that heme and HRI pathways, but not iron-regulated pathways, mediate the major protein translational and transcriptional responses to iron deficiency in erythroblasts in vivo and thereby identify previously unappreciated regulators of erythropoiesis. Our genome-wide study uncovers the major impact of the HRI-mediated integrated stress response for the adaptation to iron deficiency anemia.

2018-09-03 | GSE119365 | GEO

Human HRI Autophosphorylation Profile

Project description:Heme-regulated inhibitorRegulated Inhibitor (HRI) is one of the four mammalian kinases that phosphorylate eIF2α, facilitating a cellular response to stress through the regulation of mRNA translation. Originally identified as a heme sensor in erythroid progenitor cells, HRI has since emerged as a potential therapeutic target in both cancer and neurodegeneration. Here we purified recombinant expressed human HRI and allowed it to autophosphorylate.

2025-06-18 | PXD064940 | Pride

Effect of PTPMT1 deficiency on regulatory T cells

Project description:CD4 T cells were isolated from Wt and PTPMT1 DT mice. Cells were activated in vitro and differentiated into regulatory T cells for 4 days. At this time point WT and KO cells were harvested and analysed by proteomics.

2026-03-25 | GSE288709 | GEO

eIF2A regulates cell migration without overtly affecting translation

Project description:The RNA-binding protein eIF2A has been implicated in a variety of cellular processes including tumorigenesis. This role has been attributed to its function as alternative translation initiation factor. However, the mechanisms by which eIF2A regulates translation and its contribution to oncogenic transformation are unclear. Here, we shed light on these aspects using a melanoma cell model consisting of the non-tumoral melanocytic cell line MelST and its metastatic counterpart obtained by RasV12 overexpression (MelSTR). Depletion of eIF2A from MelST and MelSTR cells revealed acquired dependencies upon Ras transformation for migration. Surprisingly, analysis of the transcriptome (RNA-Seq) and translatome (ribosome profiling) upon eIF2A depletion showed minor to no changes in translation. RIP-Seq and RT-qPCR furthermore indicate that eIF2A binds mRNA targets in a translation-independent manner. Interestingly, protein interactome analyses point towards a function of eIF2A in cytoskeletal remodeling and indeed we can show that eIF2A localizes to the centrosome and affects its composition and orientation, linking eIF2A with migration. In addition, eIF2A promotes migration in a manner that depends on its RNA-binding activity. Together, these results indicate that eIF2A does not function as a translation factor in melanoma cells, but through a novel function which is based on its RNA-binding activity and its connections to the centrosome.

2025-06-27 | GSE279657 | GEO

PTPMT1-dependent regulatory T cells mediate immunological tolerance to gut pathobionts

Project description:Mitochondrial dysfunctions are emerging as key drivers of gut inflammation, colitis, and IBD, yet their role in regulating immune tolerance remains unclear. Meanwhile, pathobiont infections, such as those caused by Helicobacter species, affect nearly half the global population, with symptoms manifesting in only 20%, adding a new layer of complexity. The genetic and environmental factors that disrupt gut tolerogenic mechanisms, tipping the balance toward disease in symptomatic infections, are not fully understood. Here, we show that PTPMT1 impairs tolerance to Helicobacter via Treg cells, independently from T cell-generated Type I or Type II interferons. Without cardiolipin, Treg cells lose metabolic fitness and immunosuppressive potential, unleashing pro-inflammatory myeloid cells in the gut. As a result, PTPMT1 ΔT mice are highly vulnerable to pathobiont infections even without microbiome imbalance. Inflammation and helper T cell imbalance are conserved in Barth syndrome, linked to cardiolipin deficiency from TAFAZZIN mutations. Overall, we propose that T cell-specific PTPMT1 governs the balance between tolerance and inflammation in the gut, dictating outcomes in pathobiont infections.

2026-04-01 | GSE288641 | GEO

eIF2A regulates cell migration without overtly affecting translation [Ribo-Seq]

2025-06-27 | GSE279472 | GEO